Erythrocyte programmed cell death

Föller, Michael; Huber, Stephan M.; Läng, Florian

doi:10.1002/iub.106

Cited by 253 publications

(272 citation statements)

References 137 publications

(72 reference statements)

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“…Moreover, the degradation of erythrocytes involves a characteristic pathway called eryptosis, which is a version of apoptosis. These cells lack both nucleus and mitochondria, but PS externalization is also characteristic for them (Foller et al 2008).…”

Section: Aminophospholipid Asymmetry Of Plasma Membrane and Its Apoptmentioning

confidence: 99%

Beyond annexin V: fluorescence response of cellular membranes to apoptosis

2012

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Dramatic changes in the structure of cell membranes on apoptosis allow easy, sensitive and non-destructive analysis of this process with the application of fluorescence methods. The strong plasma membrane asymmetry is present in living cells, and its loss on apoptosis is commonly detected with the probes interacting strongly and specifically with phosphatidylserine (PS). This phospholipid becomes exposed to the cell surface, and the application of annexin V labeled with fluorescent dye is presently the most popular tool for its detection. Several methods have been suggested recently that offer important advantages over annexin V assay with the ability to study apoptosis by spectroscopy of cell suspensions, flow cytometry and confocal or twophoton microscopy. The PS exposure marks the integrated changes in the outer leaflet of cell membrane that involve electrostatic potential and hydration, and the attempts are being made to provide direct probing of these changes. This review describes the basic mechanisms underlying the loss of membrane asymmetry during apoptosis and discusses, in comparison with the annexin V-binding assay, the novel fluorescence techniques of detecting apoptosis on cellular membrane level. In more detail we describe the detection method based on smart fluorescent dye F2N12S incorporated into outer leaflet of cell membrane and reporting on apoptotic cell transformation by easily detectable change of the spectral distribution of fluorescent emission. It can be adapted to any assay format.

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Section: Aminophospholipid Asymmetry Of Plasma Membrane and Its Apoptmentioning

confidence: 99%

Beyond annexin V: fluorescence response of cellular membranes to apoptosis

2012

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“…Many cells exhibit transient exoplasmic protrusions, known as blebs, during several physiological processes, including cytokinesis, cell motility, apoptosis, and virus uptake [3][4][5][6][7][8][9]. Recent experiments revealed that blebs can be induced in suspended fibroblasts when these are subjected to a localized ablation of the cortical CSK [10].…”

Section: Introductionmentioning

confidence: 99%

Computer simulation of cytoskeleton-induced blebbing in lipid membranes

et al. 2011

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Blebs are balloon-shaped membrane protrusions that form during many physiological processes. Using computer simulation of a particle-based model for self-assembled lipid bilayers coupled to an elastic meshwork, we investigated the phase behavior and kinetics of blebbing. We found that blebs form for large values of the ratio between the areas of the bilayer and the cytoskeleton. We also found that blebbing can be induced when the cytoskeleton is subject to a localized ablation or a uniform compression. The results obtained are qualitatively in agreement with the experimental evidence and the model opens up the possibility to study the kinetics of bleb formation in detail.

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“…Beyond Gardos channel activation and cell shrinkage, an increase in free [Ca 2+ ] i could also lead to scramblase activation and phosphatidylserine exposure on the outer membrane leaflet. Cation channels are thus implicated in the cascade of events leading to RBCs death, a phenomenon called eryptosis (as an erythrocytic-specific apoptosis) and described by the group of Florian Lang (Foller et al, 2008a;F. Lang et al, 2006;K.S.…”

Section: Non-selective Cation Channelmentioning

confidence: 99%

“…This follows the same path: an external signal (oxidative stress, for example) triggers a rise in intracellular Ca 2+ , probably by activation of a non-selective cation channel by prostaglandin E2. This provokes cell shrinkage, scramblase and calpain activation resulting in phosphatidylserine exposure and degradation of the cytoskeleton (reviewed in (Foller et al, 2008a;F. Lang et al, 2006)).…”

Section: Senescencementioning

confidence: 99%